Objective To evaluate the feasibility of establishing a portal vein thrombosis (PVT) model in cirrhotic rats. Methods Fifty male SD rats aged 10 ~ 12 weeks and body mass about 300 ~ 350g were divided randomly into a model group and a blank group. Cirrhosis was initially established in the model group. PVT was then established by intermittent portal vein ligation with clamping, and was confirmed by hepatic color Doppler ultrasonography 1 week after modeling. The model group was then divided randomly into a model control group and a model recovery group. Liver and portal vein tissues were extracted from the model control and blank groups after laparotomy, and from the model recovery group after continued feeding for 2 weeks. Liver and portal vein samples in each group were stained with hematoxylin eosin (HE) and Masson stain and portal vein samples were stained with Elastica van Gieson (EVG) stain. Results Ultrasound examination showed stable thrombus formation in the portal vein in the model group 1 week after surgery, with a modeling success rate of 68%. HE and Masson staining showed false lobules and PVT, media edema and thickening, and collagen fiber adhesion, and EVG staining showed portal vein intimal injury in the model and model recovery groups. In contrast, there was no PVT and the vascular structure was intact in the blank group. Transmission electron microscopy showed collagen fiber bundles in the hepatic sinuses of cirrhotic rats, and hepatocyte mitochondria were heterogeneous in size, with focal aggregation. Portal vein endothelium exfoliation, apoptosis, phenotypic migration of smooth muscle cells to the protoendothelium, and subintimal fibrous tissue proliferation were also detected. No rats in the model recovery group had died 3 weeks after surgery and PVT remained stable. Conclusions Shedding of the portal vein endothelium, intimal fibrosis, phenotypic smooth muscle cells and migration to the intima are important pathologic findings of PVT in cirrhosis. Intermittent ligation combined with clamping can be used to establish a stable model of PVT in rats with liver cirrhosis, and the pathological changes, including vascular endothelial injury, intima thickening and fibrosis, and slow blood flow, are consistent with the formation mechanism of PVT in liver cirrhosis. Model rats can survive for at least 3 weeks, thus providing a suitable model and survival time for further studies of PVT in liver cirrhosis.